Faculty Bibliography

BACKGROUND:Particle matter (PM) has been associated with increased morbidity and mortality rates across the world. This study was designed to test the hypotheses that pyrotechnic firework displays introduce significant amounts of toxic metals into the atmosphere and are hazardous to human health. Size-selective emissions from 10 different fireworks displays were collected during particle generation in a dynamic, stainless steel chamber and tested for toxicity in cells. A subset of 2 particle types were tested in vivo in mice. At doses that did not produce cytotoxicity in an LDH assay, in vitro reactive oxygen species (ROS) formation was measured in bronchial epithelial airway (BEAS-2B) and human pulmonary microvascular endothelial (HPMEC-ST1.6R) cell lines treated with size-fractionated particles from the emissions of fireworks. RESULTS:sample for the fireworks type producing the greatest in vitro ROS response in BEAS-2B cells contained ~ 40,000 and ~ 12,000 ppm of lead and copper, respectively. This sample also produced the greatest inflammatory response (i.e., increased neutrophils in bronchoalveolar lavage fluid) in mice. CONCLUSIONS:These findings demonstrate that pyrotechnic display particles can produce adverse effects in mammalian cells and lungs, thus suggesting that further research is needed to expand our understanding of the contribution of metal content to the adverse health effects of fireworks particles. This information will lead to the manufacture of safer fireworks.

Air pollution is a major contributor to cardiovascular morbidity and mortality. Fine particulate matter <2.5 µm in diameter may be a modifiable risk factor for hypertension. The benefits of in-home air filtration on systolic blood pressure (BP) and diastolic BP are unclear. To examine the effects of in-home personal air cleaner use on fine particulate exposure and BP, we queried PubMed, Web of Science, Cochrane Central Register, Inspec, and EBSCO GreenFILE databases for relevant clinical trials. Included studies were limited to nonsmoking participants in smoke-free homes with active or sham filtration on indoor fine particulate concentrations and changes in systolic and diastolic BP. Of 330 articles identified, 10 trials enrolling 604 participants who met inclusion criteria were considered. Over a median 13.5 days, there was a significant reduction of mean systolic BP by ≈4 mm Hg (-3.94 mm Hg [95% CI, -7.00 to -0.89]; P=0.01) but a nonsignificant difference in mean diastolic BP (-0.95 mm Hg [95% CI, -2.81 to 0.91]; P=0.32). Subgroup analyses indicated no heterogeneity of effect by age, level of particulate exposure, or study duration. Given the variation in study design, additional study is warranted to confirm and better quantify the observed benefits in systolic BP found with personal air cleaner use.

Respiratory ailments have plagued occupational and public health communities exposed to World Trade Center (WTC) dust since the September 11, 2001 attack on the Twin Towers. The nature of these ailments is proposed to be induced by inhalation exposure to WTC particulate matter (WTC_PM), released during the collapse of the buildings and subsequent resuspension during cleanup. We investigated this hypothesis using both an in vitro and an in vivo mouse intranasal (IN) exposure model to identify the inflammatory potential of WTC_PM with specific emphasis on respiratory and endothelial tissue responses. In vitro studies identified WTC_PM exposure to be positively correlated with cytotoxicity and increased NO₂^- production in both BEAS-2B pulmonary epithelial cells and THP-1 macrophage cells. In vivo C57BL/6 mouse studies exhibited significant increases in inflammatory markers including increases in polymorphonuclear neutrophil (PMN) influx into nasal and bronchoalveolar lavage fluids (NLF and BALF), as well as increased total protein and cytokine/chemokines levels. Concurrently, NLF, BALF, and serum NO₂^- levels exhibited significant homeostatic temporal deviations with evidence of temporal aortic dysfunction in myography studies. Respiratory exposure to- and evidence -based retention of- WTC_PM may contribute to chronic systemic effects seen in mice, with resemblance to observed effects in WTC_PM-exposed human populations. Collectively, findings reported herein are reflective of WTC_PM exposure and its effect(s) on respiratory and aortic tissues, highlighting potential dysfunctional pathways that may precipitate inflammatory events, while simultaneously altering homeostatic balances. The tight interplay between these balances, when chronically altered, may contribute to- or result in- chronically diseased pathological states.

The trend of e-cigarette use among teens is ever increasing. Here we show the dysbiotic oral microbial ecology in e-cigarette users influencing the local host immune environment compared with non-smoker controls and cigarette smokers. Using 16S rRNA high-throughput sequencing, we evaluated 119 human participants, 40 in each of the three cohorts, and found significantly altered beta-diversity in e-cigarette users (p = 0.006) when compared with never smokers or tobacco cigarette smokers. The abundance of Porphyromonas and Veillonella (p = 0.008) was higher among vapers. Interleukin (IL)-6 and IL-1β were highly elevated in e-cigarette users when compared with non-users. Epithelial cell-exposed e-cigarette aerosols were more susceptible for infection. In vitro infection model of premalignant Leuk-1 and malignant cell lines exposed to e-cigarette aerosol and challenged by Porphyromonas gingivalis and Fusobacterium nucleatum resulted in elevated inflammatory response. Our findings for the first time demonstrate that e-cigarette users are more prone to infection.

Background/UNASSIGNED:Acrolein is a major component of environmental pollutants, cigarette smoke, and is also formed by heating cooking oil. We evaluated the interstrain variability of response to subchronic inhalation exposure to acrolein among inbred mouse strains for inflammation, oxidative stress, and tissue injury responses. Furthermore, we studied the response to acrolein vapor in the lung mucosa model using human primary bronchial epithelial cells (PBEC) cultured at an air-liquid interface (ALI) to evaluate the findings of mouse studies. Methods/UNASSIGNED:< 0.05) in the lung models. Results/UNASSIGNED:in the PBEC-ALI model. Conclusion/UNASSIGNED:The interstrain differences in response to subchronic acrolein exposure in mouse suggest a genetic predisposition. Altered expression of IL-17 pathway genes following acrolein exposure in the PBEC-ALI models indicates that it has a central role in chemical irritant toxicity. The findings also indicate that genetically determined differences in IL-17 signaling pathway genes in the different mouse strains may explain their susceptibility to different chemical irritants.

BACKGROUND:Tobacco remains the leading cause of preventable death in the United States, with 41,000 deaths attributable to secondhand smoke (SHS) exposure. On July 30, 2018, the U.S. Department of Housing and Urban Development passed a rule requiring public housing authorities to implement smoke-free housing (SFH) policies. OBJECTIVES/OBJECTIVE:Prior to SFH policy implementation, we measured self-reported and objective SHS incursions in a purposeful sample of 21 high-rise buildings (>15 floors) in New York City (NYC): 10 public housing and 11 private sector buildings where most residents receive federal housing subsidies (herein 'Section 8' buildings). METHODS:) from low-cost particle monitors. SHS was measured for 7-days in non-smoking households (NYCHA n = 157, Section 8 n = 118 households) and in building common areas (n = 91 hallways and stairwells). RESULTS:was observed between and within buildings; on average nicotine concentrations were higher in NYCHA apartments and hallways than in Section 8 buildings (p < 0.05), and NYCHA residents reported seeing smokers in common areas more frequently. CONCLUSIONS:SFH policies may help in successfully reducing SHS exposure in public housing, but widespread pre-policy incursions suggest achieving SFH will be challenging.